Key result
Increased intracranial pressure caused an increase in blood pressure from 63.2 to 128.8 mmHg and CAVI from 4.02 to 4.9, which was mediated by the autonomic nervous system and suppressed by hexamethonium.
Why the study?
Stroke leads to hypertension, but the role of vascular function and the mechanism underlying increased arterial stiffness following stroke remain unclear.
Does hexamethonium prevent the increase in blood pressure and cardio-ankle vascular index induced by enhanced intracranial pressure in rabbits?
Does hexamethonium prevent the increase in blood pressure and cardio-ankle vascular index induced by enhanced intracranial pressure in rabbits?
Increased intracranial pressure enhances arterial stiffness and blood pressure via autonomic nervous system activation, which can be suppressed by ganglionic blockade.
Answers are grounded in this paper and cite their sources.
Hexamethonium blunts ICP-induced BP and CAVI rises in rabbits; hypothesis-generating for autonomic modulation in intracranial hypertension.
AIM: Stroke is well known to lead to hypertension; nevertheless, the role of vascular function in hypertension remains unclear. In this study, we aimed to clarify the mechanism underlying increased arterial stiffness following stroke. METHODS: The cardio-ankle vascular index (CAVI) was measured in five New Zealand White rabbits. Under general anesthesia, intracranial pressure (ICP) was increased by injecting saline (15 mL) into the cisterna magna. ICP was monitored using a catheter inserted into the subarachnoid space via right frontal bone craniotomy. Blood pressure (BP), CAVI, and common carotid flow (CCF) were evaluated, and the responses of these parameters to increased ICP were analyzed. RESULTS: Saline injection into the cisterna magna increased the ICP by over 20 mmHg. Both BP and CAVI increased from 63.2±4.84 to 128.8±14.68 mmHg and from 4.02±0.28 to 4.9±0.53, respectively. Similarly, BP and CCF increased. When hexamethonium was administered before the increase in ICP, the increase in BP (132.2±9.41 mmHg with 10 mg/kg hexamethonium vs. 105.6±11.01 mmHg with 100 mg/kg hexamethonium) and CAVI (5.02±0.64 with 10 mg/kg hexamethonium vs. 4.82±0.42 with 100 mg/kg hexamethonium) were suppressed in a dose-dependent manner. CONCLUSION: Increased ICP causes an increase in BP and CAVI, suggesting that enhanced stiffness of the muscular arteries contributes to high BP. Blocking the autonomic nervous system with hexamethonium suppresses the increase in BP and CAVI, indicating that these increases are mediated by activation of the autonomic nervous system.
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Miyazaki et al. (2021) studied Increased intracranial pressure (n=5). Increased intracranial pressure via saline injection vs. Baseline (before injection) was evaluated on Systolic blood pressure (p=<0.05). Increased intracranial pressure caused an increase in blood pressure from 63.2 to 128.8 mmHg and CAVI from 4.02 to 4.9, which was mediated by the autonomic nervous system and suppressed by hexamethonium.
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